Treatment of flax cotyledons with solutions of bromacil, ioxynil, metribuzin, and monuron resulted in a rapid inhibition of CO2 fixation. Chloroplasts isolated from cotyledons treated with the above herbicides exhibited electron transport activity for some time after CO2 uptake in the intact cotyledons had ceased. However, the action of the herbicides was to decrease photosystem two (PSII) activity faster than photosystem one (PSI) activity but there appeared to be no differential breakdown of the pigment complexes resolved by polyacrylamide gel electrophoresis. Carotenoid breakdown, particularly α- and β- carotene, preceded chlorophyll loss following herbicide treatment. Ethane generation, an indicator of membrane breakdown, increased as the pigment levels decreased. Incubation of cotyledons in an argon atmosphere reduced the rate of pigment loss with ioxynil treatment and prevented pigment breakdown with monuron treatment. Pigment loss was also reduced by the addition of a singlet oxygen quencher, l, 4-diazo-bicyclo(2, 2, 2)octane (DABCO). Ultrastructural effects commenced with a rapid swelling of the chloroplast followed by a gradual disorganization and swelling of the thylakoid system and subsequent tonoplast rupture. With ioxynil numerous membrane-bound vesicles were formed in the chloroplast prior to envelope rupture. The evidence suggests that, following inhibition of electron transport, the photosynthetic inhibitor herbicides exert their toxic effect by causing the formation of excited singlet oxygen. It is suggested that this is initially quenched by the chloroplast protective mechanisms; however, since these systems are overloaded subsequent membrane breakdown occurs.
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